TGF-beta 1 and IGF-1 expression in atrophic post-menopausal endometrium

Giuseppe Loverro, Elda Perlino, Eugenio Maiorano, Gennaro Cormio, R Ricco, Ersilia Marra, Luigi Nappi, Teresa Giannini, Luigi Selvaggi, L. Selvaggi
In: Maturitas · 1999 · vol. 31(2) , pp. 179–184 · doi:10.1016/s0378-5122(98)00095-4 · PMID:10227013 · W2089672374
article OA: closed CC0 ⤵ 3 in-corpus citations
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This study investigated the expression levels of TGF-beta 1 and IGF-1 in atrophic endometrium from post-menopausal women.

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Abstract

ObjectivesEndometrial cells may synthetize cytokines and growth factors which may modulate some of the molecular mechanisms of endometrial proliferation and differentiation.Patients and methodsWe investigated the role of transforming growth factor beta-1 (TGF-beta 1), insulin-like growth factor-1 (IGF-1) and relative receptors in five tissue samples from atrophic post-menopausal endometria. The control group was represented by proliferative and secretory endometria from 10 healthy, normally-menstratued women. TGF-beta 1 and IGF-1 m-RNA expression was evaluated by Northern hybridization analysis, while TGF-beta 1 and IGF-1 receptors distribution was studied by immunohistochemistry.ResultsIn atrophic endometria Northern hybridization analysis showed a significant decrease of IGF-1 expression, and an increase of TGF-beta 1 expression compared to proliferative and secretory endometria. By immunohistochemistry it was demonstrated that TGF-beta 1 and IGF-1 receptors were both localized in cell cytoplasm, mainly in the stromal compartment.ConclusionsThe results of our study would suggest a possible role of IGF-1 and TGF-beta 1 in maintaining the quiescent differentiative state of atrophic post-menopausal endometrium. The persistence of IGF-1 and TGF-beta 1 receptors in epithelial compartment could play a key role in proliferative response of atrophic endometrium to exogenous hormone replacement therapy (HRT) or endogenous intervening high estrogens levels.

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